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Topiramate – review of selected papers

Andrzej Klimek

Affiliation and address for correspondence
AKTUALN NEUROL 2013, 13 (2), p. 88–95
Abstract

Epilepsy is one of the most wide spread and serious paroxysmal disorders as well as 30% cases of resistant epilepsy. Topiramate (TPM) is one of many drugs of the second generation. Topiramate, a sulfonatesubstituted derivative of the monosacharide D-fructose, has been associated with a broad spectrum of antiepileptic activity. The precise mechanism of TPM is unknown, is considered that TPM produce antiepileptic effects through enhancement of GABA-erge activity, inhibition of kainate/AMAP glutamate receptors, inhibition of voltage- sensitivite sodium and calcium channel, increases in potasium conductance and inhibition of carbonic anhydrase. Oral TPM is rapidly absorbed in patients with epilepsy with a relative bioavailability of near 80%. In many clinical trials, appeareddosages (i.e. 200 mg b.d.) of topiramate as monotherapy or adjunctive therapy were effective in reducing the frequency of seizures in patients with primary generalised tonic-clonic seizures, partial seizures. The cost-utility analysis included direct medical and social services cost in the UK, TPM was predicted to be cost-effective relative to standard treatment with valproic acid in adults with generalised or unclassified epilepsy cross a range of thresholds for the cost per quality-adjusted life-year (QALY) gained as was preferred over lamotrigine. However, in adults with partial epilepsy, lamotrigine appeared to be cost-effective relative to standard treatment with carbamazepine over gabapentin and topiramate. Treatment with topiramate is commonly associated with adverse events, among others especially with weight-loss and cognitive dysfunction. The carbonic anhydrase inhibitory effects of TPM may result in metabolic acidosis, renal calculi and hypohidrosis.

Keywords
epilepsy, topiramate, pharmacokinetic properties, therapeutic efficacy, adverse events

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